Chick skeletal muscle myogenesis is chosen as a model system in which to study the final regulatory transitions--directly leading to expression of the differentiated phenotype--in cytodifferentiation. These transitions might include changes in the sequestration of genetic information (in either active or inactive chromatin) and thus its availability for transcription. Alternately, they could involve only the expression of genes already sequestered in active chromatin. I will concentrate on the regulation of the structure and activity of a single gene--that coding for the skeletal muscle myosin heavy chain (MHC) during myoblast cytodifferentiation. Although chromatin has been fractionated into putative "active" and "inactive" components, possible changes in gene structure (shifts from "inactive" to "active" chromatin) during development have not been documented. I will use a complementary DNA copy of purified myosin heavy chain (MHC) mRNA as a highly selective hybridization probe to detect the MHC gene to chromatin fractions isolated from cells at selected stages in myogenesis. The thymidine analog, 5-BrdU, a specific inhibitor of myogenesis, alters general chromatin structure by altering the strength of DNA-protein interactions. The effect of 5-BrdU on the structure of the MHC gene will be analyzed.